Grand Rounds Feb

GRANDROUNDS

Daryl Ann U. Baclay-Valdehuesa, M.D.

General Data • P. S. • 57 year old • Male • Filipino • Lupa, Sta. Barbara, Iloilo

OBJECTIVES • To present a case of Top of the Basilar Syndrome. • To present its clinical symptoms, management and prognosis. • To present its incidence in the local setting.

Chief Complaint Decreased in Sensorium

History of Present Illness 3 daysPTA

(+) Fever (+) Flank Pain (+) Cough sought consult – given unrecalled meds

ADMITTED

History of Present Illness 2 Hrs PTA

(+) Snoring Unresponsive

ADMITTED

Past Medical History • Known Hypertensive – Metoprolol – poorly compliant

• Non diabetic, Non asthmatic • No known food or drug allergy • Previous Hospitalization for Pneumonia

Personal History • Smoker: 20 pack years • Occasional Alcoholic Beverage Drinker • No known food or drug allergy • Unemployed

Family History • Father – hypertensive • Mother – diabetic

Physical Examination • Unconscious, afebrile, not in respiratory distress • Vital Signs: • Anicteric sclerae, pinkish conjunctivae • No neck vein engorgement, no cervical lymphadenopathy

Physical Examination • Symmetrical chest expansion, harsh breath sounds, no wheeze, no rales • Adynamic precordium, PMI at 5th ICS anterior axillary line, no heaves, no thrills, normal rate, regular rhythm, no murmur • Flat abdomen, normoactive bowel sounds, no mass palpated • No bipedal edema, full pulses

Physical Examination • NEUROLOGIC EXAMS – GCS 6 (M4V1E1) – Isocoric pupils equally reactive to light and accomodation – (+) Corneal reflex, OU – No facial assymmetry – No gag reflex – No nystagmus, no Doll’s eye

Physical Examination 0/5

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ADMITTING IMPRESSION • T/C Cerebrovascular Disease, prob Brainstem Infarct • T/C Septic Encephalopathy sec to Pneumonia • Community Acquired Pneumonia- Moderate Risk • Hypertensive Cardiovascular Disease

At the ER • CBG – 103mg% • Venoclysis started : PNSS 1L x 80 cc/hr • #ABG • Intubation done • Hook to mechanical ventilator

At the ER • Laboratories Requested 12 leads ECG CBC, platelet count, CT, BT, Protime Na+, K+, creatinine, SGPT, uric acid Blood typing, Rh typing ETA G/S, C/S, KOH Chest x-ray PA Urinalysis

At the ER

• Medications

Citicholine 1 gm IVTT stat dose then q12H Tranexamic acid 500mg IVTT q 8H Piperacillin-Tazobactam 4.5gm IV ANST as loading dose then 2.25mg IVTT q 8H. In line nebulization with Salbutmol 1 nebule q 8H Ambroxol 1 amp IVTT q 8H Ranitidine 50mg IVTT q8H Lactulose 300cc OD at HS

2 hours after admission • Problem • Temp • Plan RTC

: (+) Fever : 38 C- 38.4 C : Paracetamol 300mg IVTT given then q4H

3 hours after admission • Problem : (+) Fever • GCS 6 (m4v1e1) T: 38 C- 39 C • (+) pinpoint pupils bilateral • (-) corneal reflex, OU • (+) Babinski reflex bilateral

• Cranial CT scan • Referred to a neurologist • Mannitol 150cc IV bolus given then 100 cc q 8H • Vitamin K 1 amp IV q 8H started

3 hours after admission • A/I : Top of the Basilar Syndrome P : Clopidogrel 75 mg/tab i tab OD : Aspirin 80mg/tab i tab OD Ideally for Intraarterial Thrombolytics Folks opted for no resuscitation

10 hours after admission • GCS3 (m1v1e1) • (-) Corneal reflex, OU • T : >42 C • Pronounced dead after 10 hrs and 30 minutes hospital stay

DISCUSSION

ANATOMY and PHYSIOLOGY • BASILAR ARTERY – Most important artery in the posterior circulation – Formed at the pontomedullary junction by the confluence of both vertebral arteries. – Lies on the ventral surface of the pons

Circle of Willis

ANATOMY and PHYSIOLOGY • BASILAR ARTERY – Branches • Anterior Inferior Cerebellar Artery • Posterior Cerebral Artery • Superior Cerebellar Arteries

Circle of Willis

ANATOMY and PHYSIOLOGY • BASILAR ARTERY • Anterior Inferior Cerebellar Artery – Lateral pontine tegmentum – Brachium pontis or middle cerebellar peduncle – Flocculus, anterior cerebellum

• Posterior Cerebral Artery – Terminal branch – Midbrain, thalamus, medial aspect of the temporal and occipital lobes

• Superior Cerebellar Arteries – Lateral aspect of the pons and midbrain – Superior surface of the cerebellum

Circle of Willis

TOP of the BASILAR SYNDROME • Normally, blood flows in an anterograde fashion from the vertebral arteries to the basilar artery up to its terminal branches

ANATOMY and PHYSIOLOGY • Normally, blood flows in an anterograde fashion from the vertebral arteries to the basilar artery up to its terminal branches

Circle of Willis

III IV V VI VII

VII

HYPOTHALAMUS

Basilar Artery Stroke: Historical Note • 1868 – 1st clinicopathologic report of basilar artery occlusion by Hayem • 1882 – Leyden presented that patients with sudden onset of bulbar signs,and were presumed to have basilar thrombosis • 1946 – Kubik & Adams’ classic report on Basilar Artery Occlusion • Early loss of consciousness • Common bilateral involvement • Combinations of pupillary disturbance, ocular and other cranial nerve palsies, dysarthria, extensor plantar reflexes,hemiplegia or quadriplegia and often marked remission of symptoms.

Basilar Artery Stroke: Historical Note • 1980 – Caplan described the “ Top of the Basilar Syndrome” which is the embolic occlusion of the distal basilar artery producing ischemia of the rostral brainstem and the posterior cerebral territories.

Top of the Basilar Syndrome • Race – African-American, Asian – more frequent

• Sex – Male to Female Ratio: 2:1

• Age – Most prevalent in the 6th and 7th decade – Occlusion of the Distal Basilar Artery is usually secondary to embolism – 4th decade – Women are typically older than men

Top of the Basilar Syndrome • History – Stuttering or progressive course of symptoms or TIAs in the vertebrobasilar territory is seen. – 50% of patients- (+) TIAs or waxing and waning of course over several days to weeks prior to occlusion.

Top of the Basilar Syndrome • History – Heralding symptoms • Motor deficits (hemiparesis/tetraparesis or facial paresis) – 40-67% • Dysarthria and speech impairment -30 – 63% • Vertigo, nausea or vomiting – 54 – 73% • Headache – 40- 42% • Visual disturbances – 21 – 33% • Altered consciousness – 17 – 33%

Basilar Artery Occlusion •

Based on the temporal profile, may manifest in 3 different ways: 1. Sudden onset of severe motor and bulbar symptoms with reduced consciousness. 2. Gradual or stuttering course of posterior circulation symptoms that finally become progressively disabling or reduce consciousness 3. Prodromal symptoms including double vision, dysarthria, vertigo and paresthesia

Basilar Artery Occlusion • •

•

Infrequent and catastrophic disease Gravest form of posterior circulation strokes that account for about 20% of ischemic strokes. Mortality : 85 to 85%

Basilar Artery Occlusion • Locked-In-Syndrome – Infarction of the basis pontis secondary to occlusive disease of the proximal and middle segments of the basilar artery -> QUADRIPLEGIA – (+) Spared level of consciousness, preserved vertical eye movements and blinking

Basilar Artery Occlusion • Top-of-the-Basilar Syndrome – Manifestation of the upper brainstem and diencephalic ischemia. – Occlusion of the rostral basilar artery usually by an embolus. – (+) changes in level of consciousness,(+) 3rd nerve palsy and pupillary abnormalities

Laboratory Studies • • • • • •

CBC Electrolytes BUN Creatinine Protime with INR and APTT Lipid profile.

Imaging Studies • CT-scan – Sensitivity of nearly 95% for identifying hemorrhage – Low sensitivity for early ischemia

• MRI and MRA – Are more sensitive

• Transcranial Doppler – 72% sensitivity and 94% specificity in patients with basilar artery disease

Other Tests • Electrocardiography – The prevalence of coronary disease is high in patients with cerebrovascular disease. – Of patients with acute stroke,5-20% have an arrhythmia. – 2-3% have a myocardial infarction. – The presence of arrhythmias has an impact on the long term management plan for stroke prevention.

• Echocardiography

Other Tests • Catheter angiography – Done to • Establish the type of vascular lesion and the mechanism of the stroke and, if early enough. • Establish if acute intervention is needed to achieve recanalization.

Neuroprotection

Neuroprotection

Neuroprotection

Neuroprotection

Neuroprotectants

Hemodynamic Management

• Goal is to minimize ischemic injury • Cerebral ischemia results in impaired autoregulation. • MAP is critical in maintaining cerebral blood flow. • Treat if SBP is >220mmHg and DBP is > 120 mmHg.

Hemodynamic Management

• Hypertension should not be treated unless the patient has evidence of acute end organ damage such as: – Hypertensive encephalopathy – Unstable Angina – Acute MI – Heart Failure – Acute Renal Failure

Hemodynamic Management • Preferred anti-hypertensive agents are Nicardepine and Labetalol. • Blood pressure treatment should be considered when thrombolytic therapy is to be administered with target BP of DBP < 110 mmHg and SBP at less than 185 mmHg.

Hemodynamic Management • Hypotension – Maintain intravascular volume by administering isotonic solutions. – Use vasopressors if MAP continues to be low. – Vasopressors such as dopamine, dobutamine or phenylephrine should be used.

Respiratory Management

• Early assessment and management of the airways is vital, given the frequent involvement of lower cranial nerves and impairment of consciousness in patients with brainstem ischemia. • Endotracheal intubation is recommended in patients with a decreased level of consciousness

Thrombolysis • Tissue Plasminogen activator (tPA) is the only pharmaceutical agent approved for treatment of acute ischemic stroke within the first 3 hours of onset. • NINDS study revealed that there is no statistically significant difference in 3-month mortality between the treatment group and placebo group.

Intravenous Thrombolysis

• Intravenous tissue plasminogen activator is the only approved treaatment for acute ischemic stroke with a number needed to treat of 8 to cure one additional stroke.

Intraarterial Thrombolysis • Emerged as the therapeutic strategy despite the absence of data from randomized trials. • Disadvantage : time delay for cerebral angiography. • Theoretical advantages include: – Direct infusion of the medication into the occluding thrombus with higher local drug concentrations. – Precise depiction of the arterial anatomy including morphology of the thrombus. – Assessment of treatment effect and extent of collateral circulation

Intraarterial Thrombolysis

• Limited by the following:

– Availability of centers with an interventional neuroradiology service that operates 24 hours a day, 7 days a week. – Education of the public, general practitioners and ER physicians that newer therapies are currently available will help expedite suitable candidates to centers with neurointerventional services and stroke expertise.

Intraarterial Thrombolysis

• PROACT I Study – First randomized, double-blinded, multicenter trial in which safety, recanalization, frequency and clinical efficacy of direct IA infusion of r-proUK was compared to placebo. – Partial or complete recanalization was evident 120 minutes after treatment onset in 58%(15/26) of rproUK group vs 14%(2/14) of placebo group.

Intraarterial Thrombolysis

Intraarterial Thrombolysis

• PROACT II Study – Higher dose of r-proUK at 9mg helped improved recanalization efficiency by 26% but symptomatic ICH rate increased by 4%. – Good clinical outcomes at 90 days with r-proUK group at 40% vs 25% of control patients.

Intraarterial vs Intravenous Thrombolysis • IV thrombolysis appears to be better suited to recanalization of smaller distal emboli. • IA thrombolysis can lyse better intracranial large vessels. • Morbidity and mortality of patients treated with intra-arterial thrombolysis is not at all different from the effect of IV thrombolysis.

Other treatments • Avoiding systemic anticoagulation is recommended for the first 24H after thrombolysis • Systemic anticoagulation may be an alternative for patients with contraindications for thrombolysis

Other treatments • Anticoagulation with heparin or LMW heparanoids has been used, but no evidence shows that this has an impact on outcome. • Clopidogrel, ASA + dipyridamole – role not known • Angioplasty with or without stent placement is not known.

CONCLUSIONS • Recanalization of the basilar artery is key to successful treatmet and prognosis. • Further investigations are needed for the the time window for treatment, patient selection and best method for recanalization. – Intra-arterial thrombolysis – Mechanical thrombolysis – Combination

CONCLUSIONS • In the absence of clear evidence, treating patients in the context of a clinical trial seems most reasonable. • If such an alternative is not available and given the limited time window, then IV thrombolysis within 3 hrs seem to be a reasonable alternative.

Intraarterial vs Intravenous Thrombolysis • IV thrombolysis appears to be better suited to recanalization of smaller distal emboli. • IA thrombolysis can lyse better intracranial large vessels.

Characteristics of Patients that can be treated with rTPA • Diagnosis of ischemic stroke causing measurable neurologic deficit. • The neurological signs should not be clearing spontaneously. • The neurological signs should not be minor and limited. • Caution should be exercised in treating patient with a major deficit. • The symptoms of stroke should not be suggestive of SAH

Characteristics of Patients that can be treated with rTPA • Onset of symptoms should be < 3 hrs before beginning treatment. • No head trauma or prior stroke in previous 3 months. • No MI the previous 3 months. • No GIT or urinary tract hemorrhage in previous 27 days. • No major surgery in the previous 14 days. • No arterial puncture at a non compressible site in the previous 7 days.

Characteristics of Patients that can be treated with rTPA • No history of previous intracranial • • • • • •

hemorrhage. BP not elevated (SBP < 185 mmHg,DBP <110 mmHg) No evidence of active bleeding and trauma on examination. Not taking oral anticoagulant or anticoagulant being taken with INR < 1.5. If receiving heparin, APTT must be in normal range. Platelet count >100,000. Blood glucose > 50mg/dl.

Characteristics of Patients that can be treated with rTPA • No seizure with no residual impairments. • CT does not showmultilobar involvement (> 1/3 of cerebral hemisphere). • The family understands the potential benefit and risks of the management.

ABG • At 2lpm – pH : 7.48 – pCO2 : 63.3 – pO2 : 70.1 – HCO3 : 48.1 – BE : + 23.6 – TCO2 : 50

ABG • At 100% – pH : 7.44 – PCO2 : 52.9 – pO2 : 474.1 – HCO3 : 36.1 – BE : + 12 – TCO2 : 37.8

Cranial CT Scan

Cranial CT Scan

Cranial CT Scan

Chest X-ray

ECG • Sinus tachycardia

Laboratory Results • CBC

• Creatinine : 1.30mgs% – Hgb : 161 • Uric acid : 667.67 – Hct : 0.48 • SGPT : 50.63 – WBC : 23.3 • Na : 143.3 • Neu : 78% – Seg : 74% • K : 4.14 – Stab : 4%

• Eos : 1% • Lym : 18% • Mon : 3%

• Albumin : 39.4 • Protime activity : 60.07% – INR : 1.57

Laboratory Results • Urinalysis – Pale straw, acidic, slightly hazy, pH 1.020 – Pus cells: 4-5 – RBC : 8-10 – Sugar : negative – Albumin : +